Scientists scrutinize just two examples in Behe’s new book; find them deeply misleading

Here’s a post by biologists Nathan Lents and Arthur Hunt (Hunt’s name isn’t under the title), examining just two cases touted by Michael Behe as showing “de-evolution” in Behe’s new ID book Darwin Devolves: The New Science about DNA That Challenges Evolution. The cases involve the loss of fur pigment and changes in fat metabolism in polar bears, whose ancestors were like brown bears eating a brown-bear diet (omnivorous) and having brown or blackish coats. When darker bears encountered cold climates, their fur evolved white coloration. Polars bears also had a much fattier diet, and so their fat-processing genes evolved as well. How did this happen? As it turns out, Behe presents the story wrongly—probably deliberately.

According to these and other reviewers, Behe’s Big Claim in the book is that since nearly all adaptations are based on “broken genes”—genes that are inactivated, either by acquiring a missense or nonsense mutation, or an amino acid substitution that makes the gene product inactive—evolution by natural selection simply involves the accumulation of one broken gene after another. In that way, says Behe, evolution is “self limiting”, since when an adaptation is based on inactive genes, it can’t be reversed (“dead genes” tend to acquire more mutations that render them even deader). In other words, by accumulating successively broken genes, evolution works its way into a corner from which it can’t extricate itself by further evolution (broken genes are hard to un-break).

Behe claims that this is true for the polar bear: that the genes that turned the ancestral coat white and changed the fat metabolism were broken genes. But when you examine the paper supposedly supporting Behe’s claim, you find, argue Lents and Hunt, that about half of them don’t seem to have any damaging mutations, and that perhaps “none of the 17 most positively selected genes in polar bears are ‘damaged’.”

In fact, we can even grant Behe a figure of 50% of genes involved in adaptation being broken, and it still doesn’t matter. For if just half of genes involved in new adaptations do new or different things and are not damaged, then his thesis doesn’t work: evolution doesn’t grind to a halt. And, as I’ve said, there are lots of genetic changes that don’t involve broken genes, including duplications, mutations that affect gene regulation, and so on.

Finally, Lents and Hunt look at one gene, APOB, that’s involved in fat metabolism and has apparently changed by selection in polar bears (you can judge the past working of selection by looking at the relative number of amino acid substitutions in a protein compared to what you’d expect if there were no selection). In Darwin Devolves, Behe claims that researchers detected multiple mutations in the polar bear’s APOB gene and concluded that the new mutations were “very likely to be damaging—that is, likely to degrade or destroy the function of the protein that the gene codes for.” (That’s a quote from Behe’s book.)

But that’s not true. It’s not what the researchers concluded. Lents and Hunt looked up the 2014 Cell paper on the population genomics of polar bears, and found that the authors actually say this (Lents’s and Hunt’s emphases):

Substantial work has been done on the functional significance of APOB mutations in other mammals. In humans and mice, genetic APOB variants associated with increased levels of apoB are also associated with unusually high plasma concentrations of cholesterol and LDL, which in turn contribute to hypercholesterolemia and heart disease in humans (Benn, 2009; Hegele, 2009). In contrast with brown bear, which has no fixed APOB mutations compared to the giant panda genome, we find nine fixed missense mutations in the polar bear (Figure 5A). Five of the nine cluster within the N-terminal ba1 domain of the APOB gene, although the region comprises only 22% of the protein (binomial test p value = 0.029). This domain encodes the surface region and contains the majority of functional domains for lipid transport. We suggest that the shift to a diet consisting predominantly of fatty acids in polar bears induced adaptive changes in APOB, which enabled the species to cope with high fatty acid intake by contributing to the effective clearance of cholesterol from the blood.

Missense mutations are mutations that change the amino acid coded for by the mutated triplet of codons; these amino acid changes do not necessarily “break” or “inactive” a protein. And in the case of APOB they apparently don’t: they likely help the protein clear cholesterol from the blood. (The clustering in a functional region is already a clue that they aren’t random “breakage” mutations.) Or, as Lents and Hunt say,

Clearly, the authors do not expect the polar bear APOB to be “broken.” Rather, a bare majority of the amino acid changes are in the most important region for the clearing of cholesterol from the blood. In other words, these mutations likely enhance the function of apoB, at least when it comes to surviving on a diet high in saturated fats.

It is also worth noting that apoB does much more than clear fatty acids from the blood. It is a very large protein that has many biochemical activities and is a central player for lipid and cholesterol transport. Even if “damaging” mutations might be beneficial in one context, they could very well be harmful or lethal in another. Moreover, mice that lack apoB are not viable.

. . . To recap: 1.) There is no evidence for Behe’s claim that APOB is degraded or diminished in polar bears and everything we know about the protein from other mammals suggests the opposite. And 2.) Behe’s claim that the most common adaptive changes in polar bears are those that degrade or destroy proteins is not supported, and the evidence suggests otherwise. Those are just the errors that we found in his first example.

And yet Behe makes this bold claim:

It seems, then, that the magnificent Ursus maritimus has adjusted to its harsh environment mainly by degrading genes its ancestors already possessed. Despite its impressive abilities, rather than evolving, it has adapted predominantly by devolving. What that portends for our conception of evolution is the principal topic of this book.

Which lay reader would contest that, not having read the technical literature?

You can read your post for the data on other proteins, but Behe is clearly counting on his readers, who aren’t scientists, to take him at his word and not dig up an arcane paper on population genetics in a technical journal.

Behe always likes to argue that if an evolutionist makes one error or misrepresentation in a presentation, then the author’s whole presentation is cast into doubt—along with evolutionary theory itself. Well, what’s good for the goose is good for the panderer. Behe’s “evolution-nearly-always-works-by-breaking-genes” claim is not supported by this example, and we know of many other examples that don’t support it, either.

But why is Behe trying to make a scientific case against evolution in a “trade book” rather than in the scientific literature? Well, you know why: scientists don’t buy his claims. He thus tries to change accepted science not by appealing to scientists, but by appealing to the scientifically uneducated public. Now that may make creationists or those who doubt evolution feel better, but it’s not going to make intelligent design theory into “the dominant perspective in science” that was one of the 20-year goals of 1998’s infamous Wedge Document.

For a longer review by Lents, which tells you a bit more about Behe’s ideas in the book, click on this piece published at AIPT.com:

It’s curious that people dont want evolution to be true. It’s more or less obvious in the case of the religious fundamentalists (because it makes god redundant) but it’s less obvious why a number of secular folk dont want it to be true of humans (or, at least, of no bits we care about in humans). My suspicion is that part of it is a very primitive sense that all the things that matter (love, goodness, truth etc) can’t be matter. Thye have to be otherwordly to work (as confused as this notion is).

If there was no Adam and Eve then there is no original sin for which a savior must be sacrificed in atonement. Evolution cuts at the foundation of christianity by eliminating the sin in “he died for your sins”.

I wish that study included the US. I think the US would have worse numbers, but how much worse I’m unsure of. But your point that many religious and spiritual in the UK and Canada are sort of OK with evolution, with a spectrum of how much god helped things along, is also the case in the US. A large number of religious believers in the US profess to be OK with evolution, with the qualifiers you mention.

This mirrors my own experience. I’ve taught in religious schools (long in the past) but by far the most virulent opposition to evolution that I;ve experienced in recent years has been from secularists. “Oh, we understand evolution just fine, but it stopped at the neck”

Let’s try and be a little more fair to Michael Behe. He accepts evolution and he accepts common decent and the fact that Earth was formed billions of years ago. What he’s trying to prove in his books is that there are limits to what evolution can accomplish and since we observe that evolution surpasses those limits (according to him) then there must be an intelligent designer guiding evolution.

This idea that evolution is true but God guides it is a common belief among religious folk in all countries. They don’t reject evolution, they just think that in addition there’s a lot of room for their gods to play a role.

I think everyone is “being fair”, meaning to hold everyone to the same standards.

I think part of his schtick and that of ID proponents in general is to “accept” evolution, as a ruse to give the scientifically illiterate notion of intelligent design airtime. It is not cynical – it’s what works. Consider all the other authors with similar ideas whom we don’t pay as much attention to. He has Lenski, Dawkins, and on and on, adventitiously giving Behe attention.

Imo, what he’s trying to do is make a lot of money from people he knows are gagging for a scientific-sounding book that opposes evolution. I have no time for him at all. I’m just as disgusted with him as I am with psychics. Both use people’s credulity to feather their nests.

“Which lay reader would contest that, not having read the technical literature?”

Biggest issue is that the standard lay reader wouldn’t be able to properly understand the technical literature. I have an advanced degree in geology, and once the discussion got technical (apoB), I was no longer reading from a point of full understanding.

Therefore, I have to rely on consensus, which people that believe in ID are not interested in.

“ In that sense, says Behe, evolution is “self limiting”, since when an adaptation is based on inactive genes, it can’t be reversed (“dead genes” tend to acquire more mutations that render them even deader). In other words, by accumulating successively broken genes, evolution works its way into a corner from which it can’t extricate itself by further evolution (broken genes are hard to un-break).”

I think this passes Dennett’s rule – to explain the “opposition’s” argument (there is no opposition here, I know) in a way that would make them say “yes, that’s an excellent way of putting it”

I remember reading an article by Behe’s son(not a creationist) who said he believed his father truly believed what he wrote. Thinking about that now, I wonder to what degree one can convince oneself of things that are clearly false. Over years of struggle, he has become completely sold on a fantasy. All doubt has been erased.

Behe seems to have lifted the “devolution” meme wholesale from the Morris school of young-earth creationism, which claims that we live in a ‘fallen world’ because of Adam and Eve sinning. You know, the same postulate that says crocodiles, polar bears and sharks once were plant eaters.

Behe needs to read a good general evolution textbook. I recommend Herron and Freeman and I think Jerry likes Futuyma’s; both have examples of point mutations giving rise to adaptive traits. H and F discuss “gene co-option” in which slightly mutated genes take on entirely new functions. They use crystallin proteins that form part of the lens of the eye in eyes and have a completely different metobolic functions in other tissues as one example. I hesitate to trot out the well-worn example of the sickle cell mutation. It clearly acts as a “broken” gene when a person has two copies of the mutant gene (one from each parent), but it confers resistance to malaria when paired with a normal version of the gene. So the “broken” beta-globin gene has an adaptive function in malarial areas. Certainly, his main argument can’t be this simplistic, can it?

Point mutations in bacterial beta-lactamase gene conferring resistance to antibiotics. Point mutations in human lactase promoter ensuring lactase persistence in adulthood. Examples of beneficial mutations are legion, to quote the enemy’s favorite book. But Behe just does not want to know.

Maybe I’m missing some nuance here since I didn’t (and likely won’t) read Behe’s book, but is he really claiming, and basing his argument, that ALL point mutations that change one AA residue into any other AA residue functionally inactivates the translated protein ?! Is this really his argument here because that’s what’s coming across.
I have a PhD in biochemistry like Behe and I read the above thorough rebuttal by Lents and Hunt and it’s a very obvious thing, context of the mutations matter at multiple levels.
Am I misunderstanding something about his argument by not reading his stuff? This seems way too simplistic and a massively incorrect argument.

Behe could just read up on the lac operon in bacteria. It has been well known for decades. The number of different ways that mutations can affect its gene expression and the resulting lactose metabolism is more than enough to refute his simple-minded claims.

To the extent that Behe’s postulate is even true, one should note a selection bias in the available examples: most mutations that have effects large enough to be detected and studied are going to be “broken” genes. But if you look carefully, you can find many mutations with small effects in both directions (Dickinson, 2008, Genetics 178: 1571). R.A. Fisher famously used a slightly out of focus microscope as an analogy. A random large adjustment is certain to make things worse, but as you consider smaller and smaller adjustments you approach a limit where a random (up or down) change will improve the focus half of the time. Similarly, mutations that improve an already functioning organism are almost always going to be mutations with small effects. But these are hard to detect and study with the conventional tools of genetics. You need to look carefully at small changes in fitness.

Yes, little steps. As a non-expert interested in evolution this is one of the things about evolution that is most commonly not gotten by non-experts in my experience. That evolutionary processes almost always happen in tiny steps. So many just don’t get that a mother doesn’t give birth to a different species.

The other big thing that non-experts most often don’t get is how a whole bunch of those tiny changes accumulated over time can result in big differences. That, for example, the changes that occur to an offspring’s genome compared to the parents are no different than the differences between the genomes of a skate and a chicken, there’s just a whole lot more of them.

Behe is listed on the Lehigh web site as a full professor. Was he/is he considered a respected researcher on biochemistry when his research (if he does any) does not include intelligent design in it?

As an aside, Donna Strickland, who won the Nobel Prize for Physics last year, is still an associate professor showing you what titles are sometimes worth in relation to achievement. In an interview, she said she just never bothered to apply for full professorship. What a career killer. /s

I have not fact-checked Behe’s career myself, but someone here commented that he waited until he got tenure and virtual immunity (as long as he does not teach ID in the classroom) and only then announced that he had “seen the light”, leaving his department to pull their hair in desperation and to issue disclaimers.

Striking, yes, but neither surprising nor unexpected. After all, they are attempting to hold on to cultural power by having people continue to believe what everyone who actually understands the issue knows is wrong.

I note that the scientific literature does not lend itself to explaining complex ideas about evolution and that’s why scientists often publish trade books where they can cover the topic more thoroughly. There are quite a few examples ….

I’m not saying that Behe’s book is as good as these books; all I’m saying is that the fact that he publishes a trade book on evolution should not be held against him otherwise you would also have to criticize the following authors for publishing trade books …

“The Language of God” by Francis Collins
Finding Darwion’s God” by Kenneth Miller
“The Runes of Evolution” by Simon Conway Morris
“Evolution: A View form the 21st Century” by James Shapiro

Good point, but the IDers, as you know, have always been desirous of publishing in the peer reviewed literature, and crow in triumph when it happens (that paper you cited is a rare one, but it is flawed on several counts). At any rate, they’d LIKE to publish in the scientific literature but they can’t because their stuff is crap.

Oh, and my book Speciation, with Allen Orr, is NOT a trade book but a technical book. It was peer reviewed by three people before Sinauer accepted it, and we had to make some of the changes that the reviewers specified.

Behe appears to accept common descent and the fact that the earth is billions of years old. He has this crazy idea that God needs to intervene to help create new species or create an irreducibly complex attribute. Sort of like Newton believing God needed to intervene to keep the solar system from becoming chaotic, except Behe is no Newton.